Glucocorticoid-induced tumor necrosis factor receptor (TNFR)-related protein (GITR), also known as TNFRSF18, AITR or CD357, is expressed on regulatory T cells and is up-regulated on antigen experienced CD4+ helper cells and CD8+ cytotoxic T cells as well as activated NK cells (Stephens et al. J. Immunol. (2004) 173(8): 5008-5020; Clothier and Watts, Cytokine Growth Factor Rev. (2014)). GITR is part of a complex system of receptors and ligands that are involved in controlling T-cell activation by antigen exposure. GITR has one known endogenous ligand, GITR ligand (GITRL), that exists in a loosely trimeric form and can cluster GITR resulting in potent cell signaling events within T cells (Chattopadhyay et al. (2007) Proc. Natl. Acad. Sci. USA 104(49): 19452-19457). The interaction between GITR and GITRL results in delivery of positive co-stimulatory signals to T cells, which enhance their proliferation and activation by antigen exposure, help to promote memory cell generation and reprogram regulatory T cells; reducing their suppressive functions (Clothier and Watts, Cytokine Growth Factor Rev. (2014) January 4; Schaer et al. Curr Opin Immunol. (2012)).